Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Showing posts with label parkinsons diagnosis. Show all posts
Showing posts with label parkinsons diagnosis. Show all posts

Friday, July 11, 2025

Earwax Secretions May Help Detect Parkinson’s Disease

 What is your competent? doctors' exact protocol to detect Parkinsons early enough to stop it? Oh, incompetently doesn't have one?

 Parkinson’s Disease May Have Link to Stroke March 2017  

The latest here:

Earwax Secretions May Help Detect Parkinson’s Disease

Odors from earwax may help distinguish individuals with Parkinson’s disease (PD) from those without the condition, a new study suggests.

Researchers found that four volatile organic compounds (VOCs) in ear canal secretions significantly differed between participants with and without PD.

The compounds — ethylbenzene, 4-ethyltoluene, pentanal, and 2-pentadecyl-1,3-dioxolane — may represent potential biomarkers. An artificial intelligence olfactory (AIO)-based screening model used in the study identified those with PD with 94% accuracy.

“The accuracy of the model really surprised us,” study investigator Hao Dong, Research Center for Frontier Fundamental Studies, Zhejiang Lab, Hangzhou, China, MD, told Medscape Medical News.

However, the study was a “small-scale, single-center experiment,” he noted in a press release.

“The next step is to conduct further research at different stages of the disease, in multiple research centers, and among multiple ethnic groups in order to determine whether this method has greater practical application value,” Dong said.

The findings were published online recently in Analytical Chemistry.

Unique Odor Profile

“Our team has long been engaged in the detection of [VOCs] secreted by the human body. By chance, we came across reports on the detection of sebum VOCs for Parkinson’s,” Dong said.

Sebum, the oily substance secreted by the skin, may carry a distinct scent in individuals with PD. In a 2019 study cited by Dong, researchers noninvasively collected sebum samples from the upper backs of 64 participants. The findings suggested that samples from those with PD contained compounds associated with a unique odor profile.

Dong and his team began with a confirmatory experiment using sebum samples collected from the upper back, as in the original study. However, they found that earwax was easier to collect and had a more stable chemical composition. These findings led them to focus on earwax in the current study.

Ear wax also contains sebum. But unlike sebum on the surface of the skin, which is exposed to various factors that can degrade it, sebum on skin inside the ear canal is protected.

Dong’s study included 209 participants, 108 of whom had a diagnosis of PD. Ear canal secretions were collected from all participants using swabs and analyzed using gas chromatography-mass spectrometry.

Results showed that ear canal secretions from participants with PD contained 196 distinct VOCs compared with 168 VOCs in those without PD. Interestingly, no two participants had identical VOC profiles.

A Disease ‘Fingerprint’?

“In this case, VOC components could be used as a ‘fingerprint’ for disease identification,” the researchers wrote.

Adjusted analyses identified four VOCs that significantly differed between participants with and without PD: ethylbenzene, 4-ethyltoluene, pentanal, and 2-pentadecyl-1,3-dioxolane.

The investigators trained the AIO system using VOC data. By combining gas chromatography-surface acoustic wave sensors with a convolutional neural network (CNN) model, the AIO system achieved up to 94.4% accuracy in distinguishing participants with PD from those without.

In addition, the CNN model demonstrated a high level of performance with an area under the curve of 0.98, well above the 0.8 threshold considered strong by the researchers.

“Further enhancements to the diagnostic model could pave the way for a promising new PD diagnostic solution and the clinical use of a bedside PD diagnostic device,” the investigators wrote.

For now, Dong said the study’s takeaway message for clinicians is that “the potential of volatile organic compounds secreted by the skin as biomarkers for Parkinson’s disease has been further verified.”

‘Holds Promise’

Commenting for Medscape Medical News, Ethan G. Brown, MD, associate professor of clinical neurology and movement disorders at the University of California-San Francisco, described the study as “attention-grabbing.” 

“You wouldn’t think that ear canal secretions are that useful, but I thought this was a very interesting application I hadn’t really been familiar with,” he said. 

Brown, who was not involved in the current research, has been involved in studies assessing the alpha-synuclein seed amplification assay as an identifier for conditions such as PD. However, that assay is in cerebrospinal fluid and can only be accessed via lumbar puncture. 

“In general, we’re always looking for biomarkers in Parkinson’s disease, especially noninvasive ways to diagnose it, and this study holds a lot of promise for that. Obtaining a sample from the ear canal would be a much easier way to screen in the clinic,” he said. 

The research may offer insight into underlying metabolic processes in PD, but it also raises several unanswered questions, Brown noted.

For example, Brown questioned whether the between-group differences in VOCs might be linked to chemical exposures, microbiome changes, or behavioral factors. Given the study’s relatively small size and single-center design, he also raised the possibility of confounding variables — such as differences in mobility, diet, or medication use between participants with and without PD. 

“There’s still be a lot to work out, but I think the method they used could potentially tell us more about [PD’s] biology,” Brown said. 

However, he cautioned that it’s early days and the findings are still at the “wait and see” stage. “Hopefully we’re getting closer to a more objective way of diagnosing Parkinson’s, which I think is really necessary for developing treatments,” he concluded. 

The study was funded by the National Natural Science Foundation of China, “Pioneer” and “Leading Goose” R&D Program of Zhejiang Province, and the Fundamental Research Funds for the Central Universities. The investigators and Brown reported having no relevant financial relationships.

Sunday, April 27, 2025

New Biomarker Enables Early, Accurate Diagnosis of Parkinson’s

 With your heightened risk of Parkinsons post stroke, now your competent? doctor can determine if those Parkinson prevention protocols, they created 8 years ago actually work. Oh no, your doctor didn't create those prevention protocols? What were they thinking? Oh, not thinking at all about the sequalae of stroke! So, they were and are FUCKING INCOMPETENT!

I guess you'll have to read up on prevention yourself! I'm mainly doing coffee.
  • Parkinsons prevention (77 posts to August 2014)

  • How coffee protects against Parkinson’s Aug. 2014 

    The latest here:  

    New Biomarker Enables Early, Accurate Diagnosis of Parkinson’s

    Summary: Researchers have identified a biomarker in spinal fluid that can detect Parkinson’s disease in its early stages with over 90% accuracy. Using a patented immuno-infrared sensor (iRS) technology, they measured the misfolding of the alpha-synuclein (αSyn) protein, a key driver of the disease.

    Early diagnosis is crucial, as clinical symptoms usually appear only after severe and irreversible brain damage. Beyond diagnosis, the platform could also accelerate the development and validation of new Parkinson’s therapies.

    Key Facts:

    • Early Detection: Misfolded alpha-synuclein (αSyn) in spinal fluid predicts Parkinson’s with over 90% sensitivity and specificity.
    • Advanced Technology: The iRS platform detects protein misfolding, a method also validated in Alzheimer’s diagnostics.
    • Therapeutic Potential: The biomarker may aid in developing and testing new Parkinson’s treatments by monitoring disease progression.

    Source: RUB

    Parkinson’s disease is a neurodegenerative disorder that is usually diagnosed in its late stage on the basis of clinical symptoms, mainly motor disorders.

    By this point, however, the brain is already severely and irreparably damaged. Moreover, diagnosis is difficult and often incorrect because the disease takes many forms and symptoms overlap with other disorders.

    This shows a brain.
    Dopamine supplements can compensate for the loss and temporarily alleviate the symptoms. Credit: Neuroscience News

    Researchers from the PRODI Center for Protein Diagnostics at Ruhr University Bochum, Germany, and the biotech company betaSENSE have now discovered a biomarker in the spinal fluid that facilitates a reliable diagnosis at an early stage and can shed light on the progression of the disease and the effect of a therapy.

    They report their findings in the journal EMBO Molecular Medicine on April 25, 2025.

    Parkinson’s disease – an unstoppable condition

    Parkinson’s disease is characterized by the loss of dopaminergic nerve cells in the brain, which usually leads to increasing motor impairments as the symptoms progress. Dopamine supplements can compensate for the loss and temporarily alleviate the symptoms.

    The misfolding of the key protein alpha-synuclein (αSyn) from α-helical structures to β-sheet-rich structures plays a crucial role in the development of Parkinson’s disease.

    “These misfoldings make the protein sticky, leading to the formation of larger complexes, so-called oligomers. The oligomers then produce long fibrillar filaments and cause the aggregation of these filaments into macroscopically large Lewy bodies in the brain,” explains Professor Klaus Gerwert, founding and managing director at PRODI and CEO of betaSENSE.

    Advanced platform technology

    In two independent clinical cohorts with a total of 134 participants, the Bochum-based researchers showed that, with a sensitivity and specificity of well over 90 percent, this misfolding of αSyn in body-fluids is a viable biomarker for the diagnosis of Parkinson’s disease.

    The research was conducted using cerebrospinal fluid samples from patients at the Parkinson’s centers in Bochum (St. Josef Hospital, Professor Lars Tönges, Professor Ralf Gold) and Kassel (Paracelsus-Elena-Klinik, Dr. Sandrina Weber, Professor Brit Mollenhauer).

    The measurements were carried out using the patented iRS (immuno-infrared sensor) technology from betaSENSE GmbH.

    betaSENSE has already successfully implemented the iRS technology for diagnosing Alzheimer’s disease. In this case, it was shown that the misfolding of the biomarker Aβ can indicate the risk of Alzheimer’s dementia at a later stage with high accuracy up to 17 years before clinical diagnosis.

    “We have now transferred this approach to Parkinson’s for the misfolding of αSyn,” stresses Klaus Gerwert.

    Development of Parkinson’s drugs

    In addition to diagnostic applications, the technology can also help to develop new active substances and prove their efficacy in clinical trials.

    About this Parkinson’s disease research news

    Author: Julia Weiler
    Source: RUB
    Contact: Julia Weiler – RUB
    Image: The image is credited to Neuroscience News

    Original Research: Open access.
    Alpha-synuclein Misfolding as Fluid Biomarker for Parkinson’s Disease Measured with the iRS Platform” by Klaus Gerwert et al. EMBO Molecular Medicine

    Monday, December 16, 2024

    Accurate Parkinson’s Detection via Emotional Brain Responses

     Your competent? doctor needs this testing for you so EXACT Parkinsons prevention protocols can be initiated.

    The latest here:

    Accurate Parkinson’s Detection via Emotional Brain Responses

    Summary: A new study has achieved near-perfect accuracy in detecting Parkinson’s disease by analyzing brain responses to emotional stimuli using EEG and AI. Researchers found that Parkinson’s patients process emotions differently, struggling with recognizing fear, disgust, and surprise and focusing more on emotional intensity than valence.

    EEG data from 20 patients and 20 healthy controls was analyzed using machine learning, achieving an F1 score of 0.97 for diagnostic accuracy. This breakthrough offers a non-invasive, objective diagnostic method, potentially revolutionizing early detection and treatment for Parkinson’s disease.

    Key Facts

    • Diagnostic Accuracy: EEG-based emotional analysis achieved a 0.97 F1 score in identifying Parkinson’s.
    • Emotion Patterns: Parkinson’s patients recognize emotional arousal better than valence, often confusing opposing emotions.
    • AI Integration: Machine learning frameworks processed EEG data to differentiate patients from controls with high precision.

    Source: Intelligent Computing

    A joint research team from the University of Canberra and Kuwait College of Science and Technology has achieved groundbreaking detection of Parkinson’s disease with near-perfect accuracy, simply by analyzing brain responses to emotional situations like watching video clips or images.

    The findings offer an objective way to diagnose the debilitating movement disorder, instead of relying on clinical expertise and patient self-assessments, potentially enhancing treatment options and overall well-being for those affected by Parkinson’s disease.

    This shows a woman and brain waves.
    he patients were also found to struggle most with recognizing fear, disgust and surprise, or to confuse emotions of opposite valences, such as mistaking sadness for happiness. Credit: Neuroscience News

    The study was published Oct. 17 in Intelligent Computing, a Science Partner Journal, in an article titled “Exploring Electroencephalography-Based Affective Analysis and Detection of Parkinson’s Disease.”

    Their emotional brain analysis focuses on the difference in implicit emotional reactions between Parkinson’s patients, who are generally believed to suffer from impairments in recognizing emotions, and healthy individuals.

    The team demonstrated they can identify patients and healthy individuals with an F1 score of 0.97 or higher, based solely on brain scan readings of emotional responses.

    This diagnostic performance edges very close to 100% accuracy from brainwave data alone. The F1 score is a metric that combines precision and recall, where 1 is the best possible value.

    The results show that Parkinson’s patients displayed specific emotional perception patterns, comprehending emotional arousal better than emotional valence, which means they are more attuned to the intensity of emotions rather than the pleasantness or unpleasantness of those emotions.

    The patients were also found to struggle most with recognizing fear, disgust and surprise, or to confuse emotions of opposite valences, such as mistaking sadness for happiness.

    The researchers recorded electroencephalography — or EEG — data, measuring electrical brain activity in 20 Parkinson’s patients and 20 healthy controls.

    Participants watched video clips and images designed to trigger emotional responses.

    After the recording of EEG data, multiple EEG descriptors were processed to extract key features and these were transformed into visual representations, which were then analyzed using machine learning frameworks such as convolutional neural networks, for automatic detection of distinct patterns in how the patients processed emotions compared to the healthy group.

    This processing enabled the highly accurate differentiation between patients and healthy controls.

    Key EEG descriptors used include spectral power vectors and common spatial patterns. Spectral power vectors capture the power distribution across various frequency bands, which are known to correlate with emotional states.

    Common spatial patterns enhance interclass discriminability by maximizing variance for one class while minimizing it for another, allowing for better classification of EEG signals.

    As the researchers continue refining EEG-based techniques, emotional brain monitoring has the potential to become a widespread clinical tool for Parkinson’s diagnosis.

    The study demonstrates the promise of combining neurotechnology, AI and affective computing to provide objective neurological health assessments.

    About this Parkinson’s disease, emotion, and AI research news

    Author: Xuwen Liu
    Source: Intelligent Computing
    Contact: Xuwen Liu – Intelligent Computing
    Image: The image is credited to Neuroscience News

    Original Research: Open access.
    Exploring Electroencephalography-Based Affective Analysis and Detection of Parkinson’s Disease” by Ramanathan Subramanian et al. Intelligent Computing

    Sunday, November 3, 2024

    New Blood Test Shows Promise for Early Parkinson’s Detection

     

    With your risk of Parkinsons post stroke, you'll have to hope your doctor knows about this research and has a protocol created to test for this so you can get parkinson prevention protocols initiated. You better ask about that NOW before you need it. Do you have a functioning stroke doctor that will ensure these protocols get done? NO? Why are you seeing them?

    The latest here:

    New Blood Test Shows Promise for Early Parkinson’s Detection

    Summary: Researchers have developed a method to analyze extracellular vesicles (EVs) in blood for early detection of Parkinson’s disease (PD). By isolating EVs and assessing their contents, the team identified a protein called phosphorylated α-synuclein that appears in elevated levels in PD patients.

    This discovery could allow for earlier diagnosis, as these protein changes are detectable before clinical symptoms appear. The approach uses an ultra-sensitive assay that can distinguish disease markers within EVs from those free in plasma.

    If successful, this technique could enable non-invasive, blood-based diagnostics for PD and other neurodegenerative disorders. Ongoing work will determine if the test can reliably differentiate PD from other conditions.

    Key Facts:

    • Elevated phosphorylated α-synuclein levels in EVs correlate with PD progression.
    • Extracellular vesicles protect protein biomarkers, helping preserve disease indicators.
    • This blood-based diagnostic technique may enable earlier, non-invasive PD detection.

    Source: Wyss Institute

    Brain disorders like Parkinson’s (PD) or Alzheimer’s Disease (AD) start to develop in patients much earlier than when their first clinical symptoms appear.

    Treating patients at these early stages could slow or even stop their disease, but there is currently no way to diagnose brain disorders at those pre-symptomatic stages.

    Thus far, the specific brain lesions caused by PD, for example, can only be detected by analyzing brain biopsies, which can only be obtained posthumously. 

    This shows blood vials.
    Analyzing a cohort of patient samples, they could detect an enrichment of the pathological ⍺-synuclein protein inside EVs relative to total plasma. Credit: Neuroscience News

    To overcome this critical bottleneck, researchers have been pursuing the new concept of “liquid biopsies,” which involves the easy extraction of blood or other body fluids using non-invasive procedures, and analyzing them for molecules originating from brain and other solid tissues.

    A particularly promising target in body fluids are “extracellular vesicles” (EVs), tiny membrane-bound sacs released by brain and other cells into their surrounding fluids.

    These sacs contain a variety of molecules that can be unique to the cells types that produce them, such as the brain, and thus could also carry protected biomarkers for the early onset of Parkinson’s and other brain diseases. 

    However, despite recent progress, EV experts haven’t been able to tackle the problem of whether particular biomarker molecules that they measured in isolated EVs are strictly contained inside EVs or non-specifically bound to their surface.

    This challenge has actually prevented them from being able to make unambiguous conclusions about cargo molecules in EVs from all types of tissues.

    Now, a collaborative team led by David Walt, Ph.D. at the Wyss Institute at Harvard University and Brigham and Women’s Hospital (BWH) in Boston has solved this problem by adding a crucial step to an already validated ultra-sensitive protocol.

    By enzymatically digesting all surface-bound proteins from a purified EV population, they were able to specifically home in on cargo protected inside of EVs while eliminating unspecific “contaminations.”

    Using their enhanced protocol to measure the PD biomarker ⍺-synuclein in blood, for the first time they were able to accurately determine the small fraction of any protein contained within EVs vs how much of it is present free in total blood plasma. 

    Importantly, they integrated this advance with a newly developed ultra-sensitive detection assay for a form of ⍺-synuclein that becomes increasingly phosphorylated during the progression of PD and the related condition Lewy Body Dementia.

    Analyzing a cohort of patient samples, they could detect an enrichment of the pathological ⍺-synuclein protein inside EVs relative to total plasma. The findings are published in PNAS.

    “Research on EVs in our and other groups over the last few decades has steadily advanced our understanding of their complex biology and molecular composition.

    “Yet, the isolation of pure tissue-specific EVs from body fluids like blood or the cerebrospinal fluid surrounding the central nervous system, including the brain, and validating and quantifying their true contents with precise measurements still present formidable technical challenges,” said Wyss Core Faculty member Walt.

    “Our recent work is providing a solution to help fill this technological gap, and gets us closer to being able to obtain EVs free from contamination in order to use them as rich sources for clinical biomarkers, as we show with the example of phosphorylated ⍺-synuclein.”

    Walt, who is the faculty lead of the Wyss Institute’s Diagnostic Accelerator, is also the Hansjörg Wyss Professor of Biologically Inspired Engineering at Harvard Medical School (HMS), Professor of Pathology at Brigham and Women’s Hospital, and a Howard Hughes Medical Institute Professor.

    From blood to EVs to biomarkers to diagnosis

    Especially motivated by the diagnostic promise of EVs for the early diagnosis of PD, AD, and other brain disorders, the Walt group has been systematically filling vital pieces into this technical jigsaw puzzle.

    With philanthropic support from Good Ventures, the Chan Zuckerberg Initiative, and more recently the Michael J. Fox Foundation, they previously developed a technical framework for quantifying EVs and used this quantification to compare EV isolation methods from body fluids.

    Their methodology combines a separation technique known as size exclusion chromatography (SEC) to recover most EVs from biofluids with ultra-sensitive “Simoa assays” that allowed them to count single protein molecules associated with EVs that they captured and visualized with specific antibodies.

    By now, the team has engineered Simoa assays for a variety of EV-specific biomarkers and, importantly, excluded a widely used candidate surface protein, L1CAM, as a target to isolate brain-specific EVs, which provided the field with an important course correction.

    “To answer the conceptually simple but technically challenging question of what percentage of a given protein (such as ⍺-synuclein) present in plasma is inside of EVs relative to outside, we used SEC isolation methods that we previously developed to isolate most EVs from plasma together with an optimized ‘proteinase protection assay’ where we use an enzyme to gently but efficiently chew all proteins off the surface of isolated EVs, while leaving the membrane-enclosed EV interior intact.” said co-first author Dima Ter-Ovanesyan, Ph.D., who is a Senior Scientist at the Wyss Institute and spearheads the EV project with co-first author and Postdoctoral Fellow Tal Gilboa, Ph.D.

    Also, to measure ⍺-synuclein at very low levels, Gilboa, together with Postdoctoral Fellow Gina Wang, Ph.D. and Wyss Research Assistant Sara Whiteman in the Walt lab, developed a Simoa assay for ⍺-synuclein that is much more sensitive that any previously reported assay.

    Using this assay in their protocol, the team was able to determine that most of the ⍺-synuclein in EVs isolated using their SEC protocol was protected and that this amount presented less than 5% of total blood plasma ⍺-synuclein.

    Understanding this amount is particularly important for the eventual goal of measuring ⍺-synuclein in neuron-derived EVs as EVs that originate from a specific tissue like the brain are expected to be rare relative to EVs from blood cells, where ⍺-synuclein is also expressed. 

    Importantly, in addition to their ultra-sensitive Simoa assay that enabled them to detect the normal unmodified ⍺-synuclein protein, they also developed an assay that is able to detect ⍺-synuclein that becomes phosphorylated at a specific site (pSer129) in the course of PD progression.

    “When we applied our advanced methodology to a cohort of blood samples obtained from patients with PD and Lewy Body Dementia as well as healthy control donors, we found that the ratio of phosphorylated ⍺-synuclein relative to total ⍺-synuclein was two to three-fold higher inside EVs relative to outside of EVs,” said Gilboa.

    “This was extremely exciting because it suggests that EVs may protect the phosphorylation state of proteins from circulating phosphatases that would otherwise erase this highly informative mark.”

    The team is now further exploring whether these assays could be used to differentiate PD patients from people without the disease.  

    “The work by David Walt’s team presents a technological tour-de-force that brings us closer and closer to a next-generation diagnostic platform with extraordinary potential. At this point, we are not far from using these extremely rich and telling cell-derived vesicles as a window to peak into the brains of patients without requiring surgery,” said Wyss Founding Director Donald Ingber, M.D., Ph.D., who is also the Judah Folkman Professor of Vascular Biology at HMS and Boston Children’s Hospital and the Hansjörg Wyss Professor of Biologically Inspired Engineering at Harvard’s John A. Paulson School of Engineering and Applied Sciences.

    Additional authors of the paper are George Church, Ph.D., a Wyss Core Faculty member and the Robert Winthrop Professor of Genetics at HMS and Alice Chen-Plotkin, M.D., the Parker Family Professor of Neurology at the Perelman School of Medicine at the University of Pennsylvania, Philadelphia, who have both collaborated with Walt’s group since the inception of the EV project, as well as George Kannarkat.

    Funding: The work was supported by grants from the Michael J. Fox Foundation (Grant #2021A017224), Chan Zuckerberg Initiative NeuroDegeneration Challenge Network, and Good Ventures. Gilboa is an awardee of the Weizmann Institute of Science Women’s Postdoctoral Career Development Award.

    About this Parkinson’s disease research news

    Author: Benjamin Boettner
    Source: Wyss Institute
    Contact: Benjamin Boettner – Wyss Institute
    Image: The image is credited to Neuroscience News

    Original Research: Closed access.
    Measurement of α-synuclein as protein cargo in plasma extracellular vesicles” by David Walt et al. PNAS

    Monday, April 22, 2024

    VIDEO: Skin biopsy test may help diagnose Parkinson’s, dementia

    How is your competent? doctor diagnosing Parkinsons and dementia early enough to get successful prevention protocols to work?  Is your doctor prepared with these diagnosis tests? NO? Then you don't have a functioning stroke doctor!

    Your risk of dementia, has your doctor told you of this?  Your doctor is responsible for preventing this!

    1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

    2. Then this study came out and seems to have a range from 17-66%. December 2013.`    

    3. A 20% chance in this research.   July 2013.

    4. Dementia Risk Doubled in Patients Following Stroke September 2018 

    Parkinson’s Disease May Have Link to Stroke March 2017

     

    The latest here:

    VIDEO: Skin biopsy test may help diagnose Parkinson’s, dementia

    DENVER — Nearly all study participants believed to have a synucleinopathy had the presence of alpha-synuclein in their skin samples, according to a study presented at the American Academy of Neurology annual meeting.

    “The study looked at patients with one of four synucleinopathies, which include Parkinson’s disease, multiple system atrophy, pure autonomic failure and dementia with Lewy bodies,” Christopher H. Gibbons, MD, co-founder of and scientific adviser to CND Life Sciences and a neurologist at Beth Israel Deaconess Medical Center and Harvard Medical School, said in this Healio video.

    In this study, phosphorylated alpha-synuclein, which causes these disorders, was found in more than 95% of those believed to have a synucleinopathy, he said.

    “When patients and physicians are struggling with a diagnosis, this test may offer a rapid way to help identify the underlying cause of this problem,” Gibbons said.

    Sources/Disclosures

    Collapse

    Source:

    Gibbons C, et al. Cutaneous phosphorylated alpha-synuclein deposition in dementia with Lewy bodies and mild cognitive impairment. Presented at: American Academy of Neurology Annual Meeting; April 13-18, 2024; Denver.

    Disclosures: Gibbons is co-founder of and senior scientific adviser to CND Life Sciences.

    Saturday, September 23, 2023

    Wearable Device May Detect Parkinson Disease 7 Years Before Symptom Onset

    With your risk of Parkinsons you'd better hope you have a competent doctor that knows about this and has EXACT PROTOCOLS TO PREVENT PARKINSONS. 

    Your risk of Parkinson's here:

    Parkinson’s Disease May Have Link to Stroke March 2017 (Your doctor has had 6 years to put together Parkinson's prevention protocols.)

     

    Wearable Device May Detect Parkinson Disease 7 Years Before Symptom Onset

    Reduced daytime acceleration over 1 week was associated with a clinical diagnosis of Parkinson disease up to 7 years later.

    A wearable device may be able to accurately identify individuals at an elevated risk of developing Parkinson disease (PD), according to study findings published in the journal Nature Medicine.

    To date, treatment for PD consists of symptom management, with no current disease-modifying treatments available. Furthermore, at the onset of clinical manifestations, most patients will have undergone significant neuronal degeneration of dopaminergic tracts. There remains a need for reliable biomarkers that may detect the early pathologic changes that are associated with PD.

    For the study, researchers aimed to investigate the effectiveness of digital accelerometer data as a prodromal marker for PD.

    The researchers utilized a prospective, population-based cohort, termed the UK Biobank (UKBB). Accelerometry data was collected for 103,712 individuals aged 40-69, from 2013-2016. Comparison data was compiled, exploring whether accelerometers data can accurately serve as a prodromal marker for PD, by comparison of those diagnosed with PD to unaffected control individuals. Data was also compared with other current modalities, including genetic information, blood biochemistry, lifestyle, and prodromal symptoms.

    Our results suggest that accelerometry collected with wearable devices in the general population could be used to identify those at elevated risk for PD on an unprecedented scale …

    During the 2-year time of collection, 273 participants were diagnosed with PD; an additional 196 individuals were diagnosed ≥2 years after the data collection, forming a prodromal group for comparison. When comparing data between the prodromal and diagnosed PD cases to an age- and sex-matched unaffected control individuals (1:1), there was a significantly reduced daytime acceleration profile up to 7 years before diagnosis.

    Linear regression models, when adjusted for age, sex and body mass index (BMI) for residual average acceleration, found a significant reduction of acceleration in diagnostic PD and prodromal PD when compared with unaffected control individuals. Additionally, no other investigated neurodegenerative disorders (Alzheimer disease, dystonia, all-cause dementia) were found to have a reduction in acceleration before a diagnosis, as was observed in PD. Depression, however, was the only other disorder that the researchers found to have a reduction in acceleration after diagnosis.

    Prodromal and diagnosed PD could also be identified from the general population when using average acceleration with area under the precision recall curve (AUPRC) with values of 0.05±0.04 (prevalence =0.0034) and 0.06±0.05 (prevalence =0.0046), respectively. Comparing previous modalities used to identify prodromal PD (genetics, lifestyle, blood biochemistry), accelerometry data was also shown to have a better predictive value in identifying a future diagnosis of PD.

    Of note, time dependent area under the receiver operator curve (AUROC) data identified accelerometry to be able to predict the probability of not receiving a diagnosis of PD better than any other single modality previously used; the findings highlight the ability to predict when a diagnosis of PD can be expected.

    Study limitations include accelerometry data collection being restricted to a 7-day period, limiting analysis timeframe. Additional modalities with high predictive power, such as dopamine transporter imaging and motor examinations were also not included in the study.

    The researchers concluded, “Our results suggest that accelerometry collected with wearable devices in the general population could be used to identify those at elevated risk for PD on an unprecedented scale and, importantly, individuals who will likely convert within the next few years can be included in studies for neuroprotective treatments.”

    References:

    Schalkamp AK, Peall KJ, Harrison NA, Sandor C. Wearable movement-tracking data identify Parkinson’s disease years before clinical diagnosis. Nat Med. Published online July 3, 2023. doi:10.1038/s41591-023-02440-2

    Thursday, August 10, 2023

    Aging or Parkinson’s? Here Are 13 Essential Ways You Can Tell

     

    With your risk of Parkinson's post stroke is your doctor competent enough have this in a testing protocol for you? AND THEN HAVE EXACT PROTOCOLS THAT WILL PREVENT DETERIORATION INTO FULL BLOWN PARKINSONS?

    Parkinson’s Disease May Have Link to Stroke March 2017

    Do you prefer your doctor and hospital incompetence NOT KNOWING? OR NOT DOING anything on this? And they expect to be paid for doing nothing?

    Aging or Parkinson’s? Here Are 13 Essential Ways You Can Tell

    Aging is a natural, beautiful process we should all be proud of. Every wrinkle, every word, and each gesture marks all the things we’ve been through – things that made us who we are now.

    Even when we get clumsy or we feel like we’re moving slower, it’s all part of this magical journey called life.

    Or is it?

    According to Parkinson’s Foundation, more than 60,000 Americans in our country are diagnosed with Parkinson’s disease (PD) every year. A total of 10 million people around the world are living with this illness and many are still undiagnosed. Why?

    Because Parkinson’s disease occurs in people older than 50, many of its symptoms are resembling the normal signs of aging.


    However, there are a few early signs everyone should know in order to detect the illness on time and get proper treatment. Today, we’ll reveal 13 crucial symptoms of Parkinson’s disease and how they can manifest.

    Tremors

    This is one of the key signs of Parkinson’s disease although, as we’ve mentioned earlier, it can also be a normal sign of aging. How can you tell the two apart?

    Tremors caused by early Parkinson’s include sudden twitching or shaking of the chin, hands or legs. Another particularity is that these tremors stop if the person starts moving the affected part of the body.

    Since Parkinson’s is a progressive disorder, the tremors are initially so subtle only the affected person may notice them. However, they can become more frequent and intense over time.

    Interestingly enough, tremors start manifesting only on one side of the body and extend gradually to the other side as well.

    Loss of smell

    This symptom now seems more frightening than ever since it’s also a common sign of COVID-19.

    Medically called hyposmia or olfactory dysfunction, the inability to smell can actually affect between 70-90% of people diagnosed with Parkinson’s disease. This is also one of the most common ways you can tell you have the illness especially if you’re already dealing with tremors.

    However, loss of smell can happen gradually and it can manifest itself in different ways such as:

    • Difficulty recognizing odors
    • Inability to tell the difference between different odors
    • Reduced overall sense of smell

    Right now, specialists can use a variety of tests to diagnose hyposmia, but none of them is 100% accurate.

    Note that many habits or events can alter your sense of smell, including smoking, age, and prolonged chemical exposure. Furthermore, hyposmia can also be a sign of Huntington’s disease and Alzheimer’s disease, but either way, it’s definitely worth mentioning to your doctor.

    Balance problems

    How does your doctor distinguish between balance problems from stroke and those of Parkinsons? Or hasn't your doctor even thought about solving that problem?

    Parkinson’s disease can affect many of your neuronal capacities, especially basal ganglia. These tiny nerve cells are located deep inside your brain and they’re essential for flexibility and balance.

    Unfortunately, Parkinson’s disease can gradually affect these nerve cells to the point you start losing balance.

    Specialists can diagnose this symptom through an exercise known as the ‚pull test.’ During the test, a specialist will move your shoulders backwards until you lose your balance; the time it takes for you to regain balance can let doctors know whether basal ganglia is affected or not.

    In normal individuals, it only takes one or two steps backward to regain balance, while those with Parkinson’s have a harder time standing still again.

    Difficulty walking

    How does your doctor distinguish between walking problems from stroke and those of Parkinsons? Or hasn't your doctor even thought about solving that problem?

     

    If a person starts walking strangely, you think you’d notice immediately, right?

    When it comes to early Parkinson’s disease, even this symptom might be difficult to detect. We already know that this illness can affect your balance, but it can also have a negative impact on member coordination.

    As a result, people with early Parkinson’s may start dragging their feet just a little as they walk, or they may walk slower than usual.

    As the disease progresses, walking habits also become stranger: the affected person may experience an irregular pace, such as suddenly walking faster without actually wanting to.

    Sleep problems

    If this were the only symptom of Parkinson’s, I think the majority of us would suspect we have it, right?

    Sleep problems can be caused by countless problems from physical and mental disorders to stress and unhealthy lifestyle choices. However, it can also be one of the earliest signs of Parkinson’s disease when it manifests as:

    • Sudden fatigue
    • Night terrors
    • Uncontrollable movements during sleep
    • Insomnia
    • Sleep apnea

    If you notice any of the above, the first thing you should do is check your daily schedule and physical condition to eliminate any alternative reasons.

    Facial masking

    Did you know that we need at least 12 different facial muscles just for a shy smile? Our face is a wonder mechanism when it comes to the expressions we make to describe how we feel.

    Unfortunately, though, Parkinson’s disease can also affect nerve cells in this area, which causes a symptom medically called facial masking.

    In simple terms, a person with early Parkinson’s may no longer be able to make the facial expressions they desire. As the disease progresses, they gradually lose their ability to make any face expressions, which can make them seem emotionless, as if they’re wearing a mask.

    A particularity of this symptom is that it might also cause a person to blink slower than usual.

    Parkinson’s or Bradykinesia?

    Since Parkinson’s disease can cause sudden twitches and tremors, you’d think the affected people seem very agitated all the time. However, there’s another side of the coin, medically called bradykinesia.

    This term refers to a slower movement of a certain part of the body. Some of the most common examples are hand and leg stiffness or having a hard time starting to move (think getting up from the chair or starting to walk).

    Sadly, many people dealing with this symptom never mention it to their doctor because they think it’s just due to aging. Unlike aging, though, Parkinson’s bradykinesia doesn’t reduce your bone density or muscle strength, since it only affects the nerve cells.

    Changes in handwriting

    Handwriting is a practice that requires fine motor skills – and Parkinson’s disease can have a negative impact in this case as well.

    The medical term for this symptom is micrographia, a disorder that makes the affected person’s handwriting unusually small or cramped.

    Micrographia can be a sign of many illnesses which affect the nervous system, especially neurodegenerative disorders like Parkinson’s. If you notice any strange changes in your handwriting it’s definitely worth mentioning it to your doctor.

    You should also be aware of other signs of dementia to make sure you detect them ahead of time.

    Different posture

    Unfortunately, walking isn’t the only physical activity that becomes affected by Parkinson’s disease. People in the early stages of the illness might have their posture affected as well.

    Parkinson’s can cause muscle rigidity, which might make them bend forward as if they’re hunched or stooped over. This is an involuntary gesture that’s caused by a lack of balance and reduced neuronal capacities.

    Of course, bad posture can also be a normal sign of aging; the difference is that in this case it can be corrected or adapted through practice and physical activity.

    Constipation

    With this: The incidence of constipation for stroke was 48%. 

    How is your doctor telling the cause?

    Who would’ve thought that Parkinson’s disease can cause this common digestive symptom?

    Statistically, 25% of people diagnosed with Parkinson’s disease are experiencing constipation even before any motor signs such as difficulty walking, posture problems, or facial masking.

    However, constipation can be caused by a wide range of reasons; if it happens after a Thanksgiving feast, for instance, there’s definitely no need to worry.

    However, constant constipation can be the result of an unhealthy lifestyle or a disease that affects the digestive system.

    Psychological changes

    All of these are fairly normal after a stroke.

    Aside from affecting nerve cells and neurotransmitters inside the body, Parkinson’s disease can also change the normal production of hormones such as dopamine.

    Dopamine is an essential hormone for controlling your mood and behavior daily. When it becomes affected, you may start experiencing:

    • Unexplained anxiety
    • Apathy
    • Confusion
    • Inability to solve simple problems

    As the disease progresses and hormonal production becomes more and more affected, you may also experience psychosis.

    Note that all of the symptoms listed above can signal other types of dementia as well, including Alzheimer’s disease. Discussing every change with your doctor is key to detecting any potential illness on time.

    Unexplained weight loss

    Weight loss may sound nice to most of us, but it can seriously affect your health when it’s caused by an illness.

    Although it’s not a symptom of its own, weight loss comes as a consequence of many signs brought about by Parkinson’s disease.

    One of them, for instance, is tremors; even though tremors happen involuntarily, they still require plenty of energy, which can lead to unexplained weight loss. Constipation, loss of smell, and psychological changes such as depression can also severely reduce the appetite, so you will no longer meet your daily nutritional needs.

    As the disease progresses, tremors might make the eating process even more difficult and energy-draining, which also reduces the normal meal intake.

    Speech changes

    People with an advanced stage of Parkinson’s may have a difficult time speaking due to tremors or facial masking.

    However, this symptom can also show up in the early stages of the illness in the form of a softer tone or an unusual fluctuation in volume (speaking very loud, then very softly unintentionally).

    The opposite effect is also possible: some people with early Parkinson’s can lose the ability to change their vocal tone and volume, thus speaking monotonously without any intonation.

    Luckily, this is one of the few symptoms that’s immediately noticeable both by the affected person and those around them.

    Your takeout

    Parkinson’s disease is a degenerative disorder that mostly affects the elderly population. We should all be aware of its symptoms and call the doctor as soon as we notice them in ourselves or a loved one.

    Unfortunately, many people who start experiencing these signs might feel too embarrassed to discuss them with their family or visit a specialist, so we should always pay attention to unusual changes.

    Many times, shaky hands or stiffness can simply be a normal sign of aging. However, as I always like to say, prevention is always better than treatment!

    With that in mind, I’m going to leave you a few of our top retiree resources so you can live a healthy, happy life: 10 Subtle Signs of Dementia Every Retiree Should Know


    Friday, April 14, 2023

    Parkinson's Biomarker Shows High Accuracy

    With your risk of Parkinsons you'd better hope you have a competent doctor that knows about this and has EXACT PROTOCOLS TO PREVENT PARKINSONS. 

    Your risk of Parkinson's here:

    Parkinson’s Disease May Have Link to Stroke March 2017 (Your doctor has had 6 years to put together Parkinson's prevention protocols.)

    Parkinson's Biomarker Shows High Accuracy

    Assay identifies hallmark protein and could help diagnose people earlier

    A photo of blue rubber gloved hands holding an assay plate.

    An alpha-synuclein seed amplification assay (SAA) accurately detected Parkinson's disease in cerebrospinal fluid (CSF) and identified people with early, non-motor symptoms prior to diagnosis, cross-sectional data from the Parkinson's Progression Markers Initiative (PPMIopens in a new tab or window) showed.

    Sensitivity for Parkinson's disease overall was 87.7% and specificity for healthy controls was 96.3%, reported Andrew Siderowf, MD, of the University of Pennsylvania in Philadelphia, and colleagues in Lancet Neurologyopens in a new tab or window.

    Among people with sporadic Parkinson's disease, the assay showed 93.3% sensitivity. For sporadic Parkinson's disease with the typical olfactory deficit, sensitivity was 98.6%.

    However, results varied for genetic forms of Parkinson's disease, with 95.9% sensitivity for GBA mutation carriers and 67.5% sensitivity for those with LRRK2. Some differences also were seen based on age and sex.

    Misfolded alpha-synuclein protein aggregates in the brain are a hallmark of Parkinson's disease. Earlier studies have shown that an alpha-synuclein SAA could distinguish people with Parkinson'sopens in a new tab or window from those without the disease, but before this study, no large-scale analysis addressing the heterogeneity of the disease had been conducted.

    "Recognizing heterogeneity in underlying pathology among patients with Parkinson's disease has been a major challenge," Siderowf said in a statement.

    "Identifying an effective biomarker for Parkinson's disease pathology could have profound implications for the way we treat the condition, potentially making it possible to diagnose people earlier, identify the best treatments for different subsets of patients, and speed up clinical trials," he added.

    The 1,123 participants in the study included 545 people with Parkinson's (373 with sporadic disease, 123 with a LRRK2 variant, and 49 with a GBA variant), 51 people with prodromal Parkinson's (18 with hyposmia and 33 with REM sleep behavior disorder), 310 asymptomatic carriers of Parkinson's-associated genes, 54 people with parkinsonism who had scans without evidence of dopamine deficiency, and 163 healthy controls. Study participants were recruited between July 2010 and July 2019 and came from 33 participating academic neurology outpatient practices worldwide.

    Overall, 86% of prodromal participants had positive assay results (44 of 51 people, including 16 of 18 with hyposmia and 28 of 33 with REM sleep behavior disorder). Of 310 asymptomatic carriers of Parkinson's-associated genes, 8% (9% with LRRK2 and 7% with GBA) were positive.

    The clinical feature that most strongly predicted a positive result was loss of smell. Among participants with Parkinson's disease who had hyposmia, 97.2% had a positive assay result compared with 63.0% of those whose sense of smell was unchanged.

    "While loss of smell appears to be a strong predictor of Parkinson's disease, it's important to note that this study identified individuals with positive alpha-synuclein SAA results but who had not yet lost their sense of smell, indicating that alpha-synuclein pathology may be present even before there is a measurable loss of sense of smell," observed co-author Tanya Simuni, MD, of Northwestern University in Chicago.

    "Our study looked at patients at a fixed point in time only, and further research is needed to find out how patients' sense of smell may change over time, and how this relates to the build-up of alpha-synuclein aggregates in the brain," she added.

    The findings confirm the high sensitivity and specificity of the alpha-synuclein SAA assay in distinguishing Parkinson's from healthy controls, noted Daniela Berg, MD, and Christine Klein, MD, both of University Hospital Schleswig-Holstein in Germany, in an accompanying editorialopens in a new tab or window.

    "However, the study reaches well beyond this mere confirmation," they wrote. "Siderowf and colleagues showed that people with prodromal Parkinson's disease and non-manifesting mutation carriers had abnormal alpha-synuclein aggregation before any other detectable clinical or biomarker changes, a finding that lays the foundation for a biological diagnosis of Parkinson's disease, comparable with Alzheimer's diseaseopens in a new tab or window, for which use of the ATN [amyloid, tau, and neurodegeneration] criteria can establish a diagnosis before the detection of any cognitive impairment."

    "This framework shift in diagnosis changes the possibility of therapeutic intervention to an early point in disease development," Berg and Klein added. "Moreover, because non-motor symptoms might indicate differential starting points of the neurodegenerative process, future subtype-specific interventions could be possible."

    To leverage the potential of alpha-synuclein seed amplification, the test will need to be performed in blood rather than CSF, a less invasive approach that is viable, the editorialists pointed out. "Although the blood-based method needs to be further elaborated for scalability, alpha-synuclein SAA is a game-changer in Parkinson's disease diagnostics, research, and treatment trials," they wrote.

    The study had several limitations, Siderowf and co-authors acknowledged. Some participant groups had low sample sizes, and the analysis was cross-sectional, not longitudinal.

    • Judy George covers neurology and neuroscience news for MedPage Today, writing about brain aging, Alzheimer’s, dementia, MS, rare diseases, epilepsy, autism, headache, stroke, Parkinson’s, ALS, concussion, CTE, sleep, pain, and more. Follow

    Disclosures

    The study was funded by the Michael J. Fox Foundation for Parkinson's Research and a consortium of 40 private and philanthropic partners.

    Siderowf reported consultancy for Merck and the Parkinson Study Group and honoraria from Bial. Co-authors reported numerous relationships with industry and nonprofit groups. Some co-authors were employees of Amprion, owned stock in the company, or will receive royalties from Amprion's seed amplification assay.

    Berg and Klein reported no competing interests.

    Primary Source

    Lancet Neurology

    Source Reference: opens in a new tab or windowSiderowf A, et al "Assessment of heterogeneity among participants in the Parkinson's Progression Markers Initiative cohort using α-synuclein seed amplification: a cross-sectional study" Lancet Neurol 2023; DOI: 10.1016/S1474-4422(23)00109-6.

    Secondary Source

    Lancet Neurology

    Source Reference: opens in a new tab or windowBerg D, Klein C "α-synuclein seed amplification and its uses in Parkinson's disease" Lancet Neurol 2023; DOI: 10.1016/S1474-4422(23)00124-2.